Увійти

Готові списки джерел за темами / Atrial fibrillation; stroke; thrombogenesis / Статті в журналах

Статті в журналах з теми "Atrial fibrillation; stroke; thrombogenesis"

Щоб переглянути інші типи публікацій з цієї теми, перейдіть за посиланням: Atrial fibrillation; stroke; thrombogenesis.

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 29 січня 2023

Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями

Оберіть тип джерела:

Ознайомтеся з топ-50 статей у журналах для дослідження на тему "Atrial fibrillation; stroke; thrombogenesis".

Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.

Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.

Переглядайте статті в журналах для різних дисциплін та оформлюйте правильно вашу бібліографію.

1

Goette, Andreas, and Uwe Lendeckel. "Atrial Cardiomyopathy: Pathophysiology and Clinical Consequences." Cells 10, no. 10 (September 30, 2021): 2605. http://dx.doi.org/10.3390/cells10102605.

Повний текст джерела

Анотація:

Around the world there are 33.5 million patients suffering from atrial fibrillation (AF) with an annual increase of 5 million cases. Most AF patients have an established form of an atrial cardiomyopathy. The concept of atrial cardiomyopathy was introduced in 2016. Thus, therapy of underlying diseases and atrial tissue changes appear as a cornerstone of AF therapy. Furthermore, therapy or prevention of atrial endocardial changes has the potential to reduce atrial thrombogenesis and thereby cerebral stroke. The present manuscript will summarize the underlying pathophysiology and remodeling processes observed in the development of an atrial cardiomyopathy, thrombogenesis, and atrial fibrillation. In particular, the impact of oxidative stress, inflammation, diabetes, and obesity will be addressed.

Стилі APA, Harvard, Vancouver, ISO та ін.

2

Contractor, Tahmeed, and Atul Khasnis. "Left Atrial Appendage Closure in Atrial Fibrillation: A World without Anticoagulation?" Cardiology Research and Practice 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/752808.

Повний текст джерела

Анотація:

Atrial Fibrillation (AF) is a common arrhythmia with an incidence that is as high as 10% in the elderly population. Given the large proportion of strokes caused by AF as well as the associated morbidity and mortality, reducing stroke burden is the most important part of AF management. While warfarin significantly reduces the risk of AF-related stroke, perceived bleeding risks and compliance limit its widespread use in the high-risk AF population. The left atrial appendage is believed to be the “culprit” for thrombogenesis in nonvalvular AF and is a new therapeutic target for stroke prevention. The purpose of this review is to explore the evolving field of percutaneous LAA occlusion. After briefly highlighting the risk of stroke with AF, problems with warfarin, and the role of the LAA in clot formation, this article discusses the feasibility and efficacy of various devices which have been developed for percutaneous LAA occlusion.

Стилі APA, Harvard, Vancouver, ISO та ін.

3

D’Alessandro, Elisa, Joris Winters, Frans A. van Nieuwenhoven, Ulrich Schotten, and Sander Verheule. "The Complex Relation between Atrial Cardiomyopathy and Thrombogenesis." Cells 11, no. 19 (September 22, 2022): 2963. http://dx.doi.org/10.3390/cells11192963.

Повний текст джерела

Анотація:

Heart disease, as well as systemic metabolic alterations, can leave a ‘fingerprint’ of structural and functional changes in the atrial myocardium, leading to the onset of atrial cardiomyopathy. As demonstrated in various animal models, some of these changes, such as fibrosis, cardiomyocyte hypertrophy and fatty infiltration, can increase vulnerability to atrial fibrillation (AF), the most relevant manifestation of atrial cardiomyopathy in clinical practice. Atrial cardiomyopathy accompanying AF is associated with thromboembolic events, such as stroke. The interaction between AF and stroke appears to be far more complicated than initially believed. AF and stroke share many risk factors whose underlying pathological processes can reinforce the development and progression of both cardiovascular conditions. In this review, we summarize the main mechanisms by which atrial cardiomyopathy, preceding AF, supports thrombogenic events within the atrial cavity and myocardial interstitial space. Moreover, we report the pleiotropic effects of activated coagulation factors on atrial remodeling, which may aggravate atrial cardiomyopathy. Finally, we address the complex association between AF and stroke, which can be explained by a multidirectional causal relation between atrial cardiomyopathy and hypercoagulability.

Стилі APA, Harvard, Vancouver, ISO та ін.

4

Huang, Taiyuan, Schurr Patrick, Louisa Katharina Mayer, Björn Müller-Edenborn, Martin Eichenlaub, Martin Allgeier, Jürgen Allgeier, et al. "Echocardiographic and Electrocardiographic Determinants of Atrial Cardiomyopathy Identify Patients with Atrial Fibrillation at Risk for Left Atrial Thrombogenesis." Journal of Clinical Medicine 11, no. 5 (February 28, 2022): 1332. http://dx.doi.org/10.3390/jcm11051332.

Повний текст джерела

Анотація:

Objective: Atrial cardiomyopathy (ACM) is associated with development of AF, left atrial (LA) thrombogenesis, and stroke. Diagnosis of ACM is feasible using both echocardiographic LA strain imaging and measurement of the amplified p-wave duration (APWD) in digital 12-lead-ECG. We sought to determine the thresholds of LA global longitudinal strain (LA-GLS) and APWD that identify patients with AF at risk for LA appendage (LAA) thrombogenesis. Methods: One hundred and twenty-eight patients with a history of AF were included. Left atrial appendage maximal flow velocity (LAA-Vel, in TEE), LA-GLS (TTE), and APWD (digital 12-lead-ECG) were measured in all patients. ROC analysis was performed for each method to determine the thresholds for LA-GLS and the APWD, enabling diagnosis of patients with LAA-thrombus. Results: Significant differences in LA-GLS were found during both rhythms (SR and AF) between the thrombus group and control group: LA-GLS in SR: 14.3 ± 7.4% vs. 24.6 ± 9.0%, p < 0.001 and in AF: 11.4 ± 4.2% vs. 16.1 ± 5.0%, p = 0.045. ROC analysis revealed a threshold of 17.45% for the entire cohort (AUC 0.82, sensitivity: 84.6%, specificity: 63.6%, Negative Predictive Value (NPV): 94.3%) with additional rhythm-specific thresholds: 19.1% in SR and 13.9% in AF, and a threshold of 165 ms for APWD (AUC 0.90, sensitivity: 88.5%, specificity: 75.5%, NPV: 96.2%) as optimal discriminators of LAA-thrombus. Moreover, both LA-GLS and APWD correlated well with the established contractile LA-parameter LAA-Vel in TEE (r = 0.39, p < 0.001 and r = −0.39, p < 0.001, respectively). Conclusion: LA-GLS and APWD are valuable diagnostic predictors of left atrial thrombogenesis in patients with AF.

Стилі APA, Harvard, Vancouver, ISO та ін.

5

Seo, Woo-Keun, Jin-Man Jung, Ji Hyun Kim, Seong-Beom Koh, Oh Young Bang, and Kyungmi Oh. "Free Fatty Acid Is Associated with Thrombogenicity in Cardioembolic Stroke." Cerebrovascular Diseases 44, no. 3-4 (2017): 160–68. http://dx.doi.org/10.1159/000478895.

Повний текст джерела

Анотація:

Background: Recently, the role of free fatty acids (FFAs) in thromboembolism has re-emerged in the context of cardioembolic stroke. Therefore, we attempted to determine the role of FFAs in embolic risk in various potential sources of cardioembolism (PSCE). We hypothesized that if elevated FFA levels in stroke patients are associated with thrombogenesis, then patients with a well-known high risk of embolic sources would have high FFA levels. Methods: Data collected from 2 hospital-based stroke registries were analyzed to investigate the association between FFA and PSCE. Results: A total of 2,770 acute stroke patients, including 539 with cardioembolic stroke, were selected for analysis. FFA was an independent predictor for cardioembolism (OR 2.755, 95% CI 2.221-3.417, p < 0.001). Among the PSCE, FFA levels were significantly associated with high risk of atrial fibrillation (AF), valvular heart disease, congestive heart failure with low ejection fraction, left atrial thrombus, left ventricular thrombus, left atrial smoke, and ventricular wall motion abnormality. FFA levels increased with the number of PSCE per patient without interaction with the presence of AF. Conclusions: Among acute stroke patients, FFA levels increased in groups with higher risk of cardioembolic stroke irrespective of the presence of AF. These results suggest that enhanced thrombogenicity could be the main mechanism to explain the elevated FFA levels in patients with cardioembolic stroke.

Стилі APA, Harvard, Vancouver, ISO та ін.

6

Cerveró, Jorge, Víctor Segura, Alfonso Macías, Juan Gavira, Ramón Montes, and José Hermida. "Atrial fibrillation in pigs induces left atrial endocardial transcriptional remodelling." Thrombosis and Haemostasis 108, no. 10 (2012): 742–49. http://dx.doi.org/10.1160/th12-05-0285.

Повний текст джерела

Анотація:

SummaryThe leading cause of cardioembolic stroke is atrial fibrillation (AF), which predisposes to atrial thrombus formation. Although rheological alterations promote a hypercoagulable environment, as yet undefined factors contribute to thrombogenesis. The role of the endocardium has barely been explored. To approach this topic, rapid atrial pacing (RAP) was applied in four pigs to mimic A F. Left and right endocardial cells were isolated separately and their gene expression pattern was compared with that of four control pigs. The AF-characteristic rhythm disorders and endothelial nitric oxide synthase down-regulation were successfully reproduced, and validated RAP to mimic A F. A change was observed in the transcriptomic endocardial profile after RAP: the expression of 364 genes was significantly altered (p<0.01), 29 of them having passed the B>0 criteria. The left atrial endocardium [325 genes (7 genes, B>0)] was largely responsible for such alterations. Blood coagulation, blood vessel morphogenesis and inflammatory response are among the most significant altered functions, and help to explain the activation of coagulation observed after RAP: D-dimer, 0.49 (1.63) vs. 0.23 (0.24) mg/l [median (interquartile range)] in controls, p=0.02. Furthermore, three genes directly related to thrombotic processes were differentially expressed after RAP: FGL2 [fold change (FC)=0.85; p=0.007], APLP2 (FC=-0.47; p=0.005) and ADAMTS-18 (FC=-0.69; p=0.004). We demonstrate for the first time that AF induces a global expression change in the left atrial endocardium associated with an activation of blood coagulation. The nature of some of the altered functions and genes provides clues to identify new therapeutic targets.

Стилі APA, Harvard, Vancouver, ISO та ін.

7

Park, Hyungjong, and Joonsang Yoo. "Use of Non-Vitamin K Dependent Oral Anticoagulant in Ischemic Stroke." Journal of the Korean Neurological Association 40, no. 1 (February 1, 2022): 1–14. http://dx.doi.org/10.17340/jkna.2022.1.1.

Повний текст джерела

Анотація:

Atrial fibrillation (AF) is associated with an increased incidence of ischemic stroke and transient ischemic attack. A confluence of various factors such as blood stasis, endothelial dysfunction, and prothrombotic state could be contributing to the thrombogenesis in AF. Anticoagulation is the first-line therapy for the prevention of thromboembolism by AF. In current days, non-vitamin K dependent oral anticoagulants (NOAC) are considered as the preferred choice of anticoagulants to prevent ischemic stroke in patients with AF. NOACs have comparable good efficacy and better safety with a predictable anticoagulant effect without the routine coagulation monitoring compared to vitamin K dependent oral anticoagulant. However, the proper use of NOACs needs a careful approach to many practical aspects for balancing the preventing thromboembolic events and bleeding risk. Thus, understanding the drug metabolism and indication of NOAC for a specific situation is essential. In this article, we review major clinical trials, the mechanism, and the use of NOACs in the actual clinical setting of managing ischemic stroke patients.

Стилі APA, Harvard, Vancouver, ISO та ін.

8

Regazzoli, Damiano, Francesco Ancona, Nicola Trevisi, Fabrizio Guarracini, Andrea Radinovic, Michele Oppizzi, Eustachio Agricola, et al. "Left Atrial Appendage: Physiology, Pathology, and Role as a Therapeutic Target." BioMed Research International 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/205013.

Повний текст джерела

Анотація:

Atrial fibrillation (AF) is the most common clinically relevant cardiac arrhythmia. AF poses patients at increased risk of thromboembolism, in particular ischemic stroke. The CHADS2 and CHA2DS2-VASc scores are useful in the assessment of thromboembolic risk in nonvalvular AF and are utilized in decision-making about treatment with oral anticoagulation (OAC). However, OAC is underutilized due to poor patient compliance and contraindications, especially major bleedings. The Virchow triad synthesizes the pathogenesis of thrombogenesis in AF: endocardial dysfunction, abnormal blood stasis, and altered hemostasis. This is especially prominent in the left atrial appendage (LAA), where the low flow reaches its minimum. The LAA is the remnant of the embryonic left atrium, with a complex and variable morphology predisposing to stasis, especially during AF. In patients with nonvalvular AF, 90% of thrombi are located in the LAA. So, left atrial appendage occlusion could be an interesting and effective procedure in thromboembolism prevention in AF. After exclusion of LAA as an embolic source, the remaining risk of thromboembolism does not longer justify the use of oral anticoagulants. Various surgical and catheter-based methods have been developed to exclude the LAA. This paper reviews the physiological and pathophysiological role of the LAA and catheter-based methods of LAA exclusion.

Стилі APA, Harvard, Vancouver, ISO та ін.

9

Springer, Adrian, Ruben Schleberger, Florian Oyen, Boris A. Hoffmann, Stephan Willems, Christian Meyer, Florian Langer, et al. "Genetic and Clinical Predictors of Left Atrial Thrombus: A Single Center Case-Control Study." Clinical and Applied Thrombosis/Hemostasis 27 (January 1, 2021): 107602962110211. http://dx.doi.org/10.1177/10760296211021171.

Повний текст джерела

Анотація:

Left atrial (LA) thrombus formation is the presumed origin of thromboembolic complications in patients with atrial fibrillation (AF). Beyond clinical risk factors, the factors causing formation of LA thrombi are not well known. In this case-control study, we analyzed clinical characteristics and genetic thrombophilia markers (factor V Leiden (FVL), prothrombin G20210A (FIIV), Tyr2561 variant of von Willebrand factor (VWF-V)) in 42 patients with AF and LA thrombus (LAT) and in 68 control patients with AF without LAT (CTR). Patients with LAT had more clinical conditions predisposing to stroke (mean CHA2DS2-VASc-score 3.4 ± 1.5 vs. 1.9 ± 1.4; P < 0.001), a higher LA volume (96 ± 32 vs. 76 ± 21 ml, P = 0.002) and lower LA appendage emptying velocity (0.21 ± 0.11vs. 0.43 ± 0.19 m/s, P < 0.001). Prevalence of FVL, FIIV and VWF-V mutations was not different, but in the subgroup of patients <65 years (y) there was a tendency for a higher incidence of VWF-V with a prevalence of 27% (LAT <65 y) vs. 7% (CTR <65 y, P = 0.066). These findings warrant further investigation of the VWF-V as a risk factor for LA thrombogenesis in younger patients.

Стилі APA, Harvard, Vancouver, ISO та ін.

10

Paulinska, P., A. Spiel, and B. Jilma. "Role of von Willebrand factor in vascular disease." Hämostaseologie 29, no. 01 (2009): 32–38. http://dx.doi.org/10.1055/s-0037-1616936.

Повний текст джерела

Анотація:

SummaryPlasma levels of von Willebrand factor (VWF) are increased in patients with cardiovascular risk factors. Various studies aimed to elucidate the relation of VWF with thrombo - embolic cardiovascular events, ischaemic stroke as well as with peripheral arterial occlusive disease. In the general population, there is only a weak association between VWF levels and future cardiovascular events or stroke. In contrast, VWF levels are predictive in patients with documented vascular disease. Those patients with increased VWF suffer a higher incidence of major adverse cardiac events including death. The extent of the VWF release and its levels independently predict clinical outcome in patients with acute coronary syndromes. Elevated VWF levels have also been observed in patients with atrial fibrillation compared to controls and predict outcome. This may at least in part be attributable to the association of VWF with underlying cardiovascular risk factors. Hence, VWF correlates with Framingham and CHADS stroke risk stratification score and can be used as a marker in patients with AF. However, VWF is not only a predictor; it also plays a crucial role in thrombogenesis. This fact has made VWF a promising target for research into new antiplatelet therapies that specifically inhibit VWF.This review focuses on the role of VWF in ACS, ischaemic stroke and peripheral arterial disease and the relevance of therapeutic interventions targeting VWF for ACS patients.

Стилі APA, Harvard, Vancouver, ISO та ін.

11

Liles, Jeffrey, Christopher Wanderling, Abigail M. Otto, Jordan Liles, Debra Hoppensteadt, Daneyal Syed, Sallu Jabati, Mushabbar Syed, and Jawed Fareed. "Persistent Prothrombotic State in Atrial Fibrillation Despite Use of Novel Oral Anti-Coagulants." Blood 128, no. 22 (December 2, 2016): 3832. http://dx.doi.org/10.1182/blood.v128.22.3832.3832.

Повний текст джерела

Анотація:

Abstract Background: Oral anticoagulants such as warfarin have been conventionally used for the management of atrial fibrillation (AF). Despite the effectiveness of warfarin, its use in AF patients requiring anticoagulation is suboptimal with an even greater underuse seen in elderly patients who are at higher risk of stroke. New oral anticoagulants such as rivaroxaban(R), apixaban (A), dabigitran (D) and edoxaban (E) have been approved to manage thrombotic and cardiovascular disorders including AF. The newer anticoagulants do not require continuous monitoring like warfarin and are much more convenient for patients with AF. Objective: To profile the baseline level of circulating thrombotic biomarkers plasminogen activator inhibitor (PAI-1), von Willebrand Factor (vWF), microparticle bound tissue factor (MP-TF) and prothrombin fragment 1.2 (F1.2) in patients with AF. Additionally, the effect of novel oral anticoagulants (R, A, D and E) on the levels of thrombotic biomarkers in patients with AF is assessed. Materials and Methods: Citrated blood samples were drawn from 30 patients (21 male and 9 female; mean age 59.1) prior to ablation surgery for AF at Loyola University Medical Center in Maywood, Illinois. Citrated blood was spun at 3000 rpm to obtain platelet poor plasma. Normal plasma samples from healthy controls (24 male and 24 female; mean age 33) were purchased from a commercial source (George King Biomedical, Overland Park, KS). The plasma samples were analyzed using a biochip array (Randox, London, UK) for metabolic syndrome biomarkers including PAI-1 and ELISA kits for vWF, MP-TF (Hyphen BioMed, Nueville-Sur-Oise, France) and prothrombin F1.2 (Siemens, Newark, DE). Results: Compared to the control group, circulating levels of vWF, MP-TF and PAI-1 were statistically increased in patients with AF (P<0.0001, P<0.0001, and P=0.0014, respectively). Circulating levels of prothrombin F1.2 showed no difference between the AF and the control group (P=0.2696). AF patients (n=30) were divided into two groups based on their usage (Group 1, n=17) and non-usage (Group 2, n=10) of any novel oral anticoagulant (R, A, D and E). Three patients on warfarin were excluded from this section of data analysis. A statistical increase in vWF (P=0.0018) and MP-TF (P=0.0039) remained in those taking novel oral anticoagulants compared to group 2. No difference was seen in PAI-1 (P=0.333) or F1.2 (P=0.31) between groups 1 and 2. Percent change from the normal mean was also calculated for PAI-1, vWF, MP-TF and F1.2 in group 1 (78%, 61.1%, 142%, 8.9%, respectively) and group 2 (113.6%, 16.9%, 31.7%, 41.4%, respectively) as seen in table 1. Discussion: Elevated levels of PAI-1, vWF and MP-TF seen in AF patients compared to normal provide insight into an additional risk of thrombogenesis associated with AF which is not targeted by current anticoagulant medications. Most AF patients are assessed using a stroke risk stratification scale (CHA2DS2VASc) to determine if anti-coagulants should be used to prevent stroke associated with AF. Patients in group 1 had a mean CHA2DS2VASc score of 1.15 compared to 2.18 see in group 2. This data supports studies which suggest that including levels of prothrombotic biomarkers to current risk stratification scales could be more effective in assessing the risk of stroke of patients with AF. This data also suggests that although very effective in lowering prothrombin F1.2 levels in AF, the newer anticoagulants, R,A,D and E still leave additional prothrombotic biomarkers unaffected. These unaffected biomarkers could be the potential target of future drug therapies which could lower the risk of stroke in patients with AF even more than the use of newer anticoagulants alone. Disclosures No relevant conflicts of interest to declare.

Стилі APA, Harvard, Vancouver, ISO та ін.

12

Liles, Jeffrey Paul, Christopher Wanderling, Jordan Lee Liles, Debra Hoppensteadt, Jawed Fareed, Daneyal Syed, and Mushabbar Syed. "Pre-Existence of Prothrombotic State in Patients with Atrial Fibrillation Despite Therapy with New and Traditional Anti-Coagulant Drugs." Blood 126, no. 23 (December 3, 2015): 4731. http://dx.doi.org/10.1182/blood.v126.23.4731.4731.

Повний текст джерела

Анотація:

Abstract Background: Oral anticoagulants such as warfarin (W) have been conventionally used for the management of atrial fibrillation (AF). Despite the effectiveness of W, its use in AF patients requiring anticoagulation is suboptimal with an even greater underuse seen in elderly patients who are at higher risk of stroke. New oral anticoagulants such as rivaroxaban (R) and apixaban (A) have been approved to manage thrombotic and cardiovascular disorders including AF. The newer anticoagulants do not require continuous monitoring like W does and are much more convenient for patients with AF. Objective: To profile the baseline level of circulating thrombogenic biomarkers von Willebrand Factor (vWF), prothrombin fragment 1.2 (F1+2), microparticle bound tissue factor (MP-TF) and plasminogen activator inhibitor (PAI-1) in patients with AF. Additionally, the effect of both newer (R and A) and traditional (W) anticoagulants on the levels of thrombogenic biomarkers in patients with AF will be assessed. Materials: Citrated blood was drawn from thirty AF patients prior to ablation surgery and spun at 3000 rpm to obtain platelet poor plasma. Normal plasma samples from healthy controls were purchased from a commercial source (George King Biomedical, Overland Park, KS). The plasma samples were analyzed using a biochip array (Randox, London, UK) for metabolic syndrome biomarkers including PAI-1 and ELISA kits for vWF, MP-TF (Hyphen BioMed, Nueville-Sur-Oise, France) and prothrombin F1+2 (Siemens, Newark, DE). Results: Circulating levels of vWF, MP-TF and PAI-1 were statistically increased in patients with AF compared to normal (P<0.0001, P<0.0001, and P=0.0014, respectively). Circulating levels of prothrombin F1+2 showed no difference between the AF and normal group (P=0.2696). AF patients (n=30) were divided into two groups based on their usage (Group 1, n=21) and non-usage (Group 2, n=9) of any anticoagulant. Furthermore, those on anticoagulants were divided based on their use of newer (R and A, Group 3, n=16) or traditional (W, Group 4, n=4) anticoagulants. A statistical increase in vWF (P<0.0001), MP-TF (P<0.0001) and PAI-1 (P=0.011) remained in Group 1 compared to normal while a statistical increase in prothrombin F1+2 (P=0.0343) and PAI-1 (P=0.0040) were noted in Group 2 compared to normal. vWF (P=0.0036) and MP-TF (P=0.0059) were elevated in Group 1 compared to Group 2 while prothrombin F1+2 (P=0.0697) and PAI-1 (P=0.4548) showed no difference between the two groups. Furthermore, there was no statistical difference in the level of any thrombogenic biomarker in AF patients between Group 3 (R and A) and Group 4 (W). (Table 1) Discussion: Elevated levels of vWF, MP-TF and PAI-1 seen in AF patients compared to normal provide insight into an additional risk of thrombogenesis associated with AF which is not targeted by current anticoagulant medications. Most patients are assessed using a stroke risk stratification scale (CHA2DS2VASc, CHADS2, CHADS-VASC, or CHADS) to determine if anti-coagulants should be used to prevent stroke associated with AF. Of the 30 patients examined in this study, 8/9 (89%) patients who were not on anticoagulants had a stroke risk stratification score of 0 while 20/21(95%) patients who were on anticoagulants had a score of >1. This data supports studies which suggest that adding levels of prothrombotic biomarkers to current risk stratification scales could be more effective in assessing the risk of stroke of patients with AF. This data also suggests that although very effective in lowering prothrombin F1+2 levels in AF, the newer anticoagulants, R and A, and the traditional anticoagulant, W, still leave additional prothrombotic biomarkers unaffected. These unaffected biomarkers could be the potential target of future drug therapies which could lower the risk of stroke in patients with AF even more than the use of newer/traditional anticoagulants alone.Table 1.Biomarkers of Thrombogenesis in AF and Normal GroupsGroupvWF (concentration %)Prothrombin F1+2 (pmol/L)MP-TF (pg/mL)PAI-1 (ng/mL)Normal4140 ± 919 n=46106.1 ± 52.7 n=500.38 ± 0.25 n=483.21 ± 4.13 n=25AF Group 1 Anticoagulant n=216616 ± 1173107.9 ± 61.20.93 ± 0.715.69 ± 4.15Group 2 Non-Anticoagulant n=94788 ± 1338162.5 ± 93.30.51 ± 0.136.49 ± 3.14Group 3 New Anticoagulants (R and A) n=166721 ± 1127103.5 ± 37.60.76 ± 0.345.68 ± 4.53Group 4 Traditional Anticoagulants (W) n=46387 ± 158075.2 ± 52.60.94 ± 0.335.63 ± 3.52 Disclosures No relevant conflicts of interest to declare.

Стилі APA, Harvard, Vancouver, ISO та ін.

13

Chan, Mark, Min Lin, Joseph Lucas, Arthur Moseley, J. Will Thompson, Derek Cyr, Hitoshi Ueda, Mariko Kajikawa, Thomas Ortel, and Richard Becker. "Plasma proteomics of patients with non-valvular atrial fibrillation on chronic anti-coagulation with warfarin or a direct factor Xa inhibitor." Thrombosis and Haemostasis 108, no. 12 (2012): 1180–91. http://dx.doi.org/10.1160/th12-05-0310.

Повний текст джерела

Анотація:

SummaryPlasma proteins mediate thrombogenesis, inflammation, endocardial injury and structural remodelling in atrial fibrillation (AF). We hypothesised that anti-coagulation with rivaroxaban, a direct factor Xa inhibitor, would differentially modulate biologically-relevant plasma proteins, compared with warfarin, a multi-coagulation protein antagonist. We performed unbiased liquid chromatography/tandem mass spectroscopy and candidate multiplexed protein immunoassays among Japanese subjects with non-valvular chronic AF who were randomly assigned to treatment with 24 weeks of rivaroxaban (n=93) or warfarin (n=94). Nine metaproteins, including fibulin-1 (p=0.0033), vitronectin (p=0.0010), haemoglobin α(p=0.0012), apolipoproteins C-II (p=0.0017) and H (p=0.0023), complement C5 precursor (p=0.0026), coagulation factor XIIIA (p=0.0026) and XIIIB (p=0.0032) subunits, and 10 candidate proteins, including thrombomodulin (p=0.0004), intercellular adhesion molecule-3 (p=0.0064), interleukin-8 (p=0.0007) and matrix metalloproteinase-3 (p=0.0003), were differentially expressed among patients with and without known clinical risk factors for stroke and bleeding in AF. Compared with warfarin, rivaroxaban treatment was associated with a greater increase in thrombomodulin (Δ0.1 vs. 0.3 pg/ml, p=0.0026) and a trend towards a reduction in matrix metalloproteinase-9 (Δ2.2 vs. –4.9 pg/ml, p=0.0757) over 24 weeks. Only modest correlations were observed between protein levels and prothrombin time, factor Xa activity and prothrombinase-induced clotting time. Plasma proteomics can identify distinct functional patterns of protein expression that report on known stroke and bleeding risk phenotypes in an ethnically-homogeneous AF population. The greater upregulation of thrombomodulin among patients randomised to rivaroxaban represents a proof-of-principle that pharmacoproteomics can be employed to discern novel effects of factor Xa inhibition beyond standard pharmacodynamic measures.

Стилі APA, Harvard, Vancouver, ISO та ін.

14

Bukowska, Alicja, Matthias Hammwöhner, Domenico Corradi, Wisno Mahardhika, and Andreas Goette. "Atrial thrombogenesis in atrial fibrillation." Herzschrittmachertherapie + Elektrophysiologie 29, no. 1 (December 12, 2017): 76–83. http://dx.doi.org/10.1007/s00399-017-0543-x.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

15

Akar, Joseph G., and Mark A. Marieb. "Atrial Fibrillation and Thrombogenesis." JACC: Clinical Electrophysiology 1, no. 3 (June 2015): 218–19. http://dx.doi.org/10.1016/j.jacep.2015.05.003.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

16

Cohen, Ariel, Stéphane Ederhy, and Emanuele Di Angelantonio. "Mechanisms of thrombogenesis in atrial fibrillation." Lancet 373, no. 9668 (March 2009): 1005–6. http://dx.doi.org/10.1016/s0140-6736(09)60603-6.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

17

Spence, David. "Mechanisms of thrombogenesis in atrial fibrillation." Lancet 373, no. 9668 (March 2009): 1006. http://dx.doi.org/10.1016/s0140-6736(09)60604-8.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

18

Khoo, Chee W., Suresh Krishnamoorthy, Hoong Sern Lim, and Gregory Y. H. Lip. "Atrial fibrillation, arrhythmia burden and thrombogenesis." International Journal of Cardiology 157, no. 3 (June 2012): 318–23. http://dx.doi.org/10.1016/j.ijcard.2011.06.088.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

19

Iwatsuki, Yoshiyuki, Chinatsu Sakata, and Yumiko Moritani. "YM150, An Oral Direct Factor Xa Inhibitor: Combination with Aspirin or Clopidogrel In Arteriovenous Shunt Thrombosis In Rats." Blood 116, no. 21 (November 19, 2010): 3318. http://dx.doi.org/10.1182/blood.v116.21.3318.3318.

Повний текст джерела

Анотація:

Abstract Abstract 3318 Background: YM150, an oral direct factor Xa inhibitor, is currently in clinical development for the prevention of venous thromboembolism in patients undergoing orthopedic surgery, prevention of stroke in patients with atrial fibrillation, and prevention of ischemic events after recent acute coronary syndrome (ACS). The antiplatelet agents aspirin or clopidogrel will likely be co-prescribed with YM150 in ACS. Here, we report the effects of YM150 in combination with aspirin or clopidogrel on thrombus formation, bleeding, platelet aggregation, and coagulation in rats. Methods: The antithrombotic effect was estimated in a rat arteriovenous shunt model. The shunt was formed by attaching a polyethylene tube containing a silk thread to the carotid artery and the contralateral carotid vein. Blood was allowed to circulate in this shunt for 15 min, and then the silk thread was withdrawn from the tube to assess the thrombus weight. YM150, aspirin, or clopidogrel was orally administered 0.5, 1, or 2 h before shunt formation, respectively. At the same time as shunt formation, an incision was made at the sole of the left foot using a template bleeding device (Surgicutt®) to measure bleeding time. To avoid interference with the thrombosis model, blood samples to assess platelet aggregation and prothrombin time were obtained from separate animals at the same time point as shunt formation in the thrombus study. Platelet aggregation was induced using 10 μg/mL of collagen and 5 μM of adenosine 5`-diphosphate (ADP) to assess the effects of aspirin and clopidogrel, respectively. Results: YM150 alone inhibited thrombus formation, with significance at 10 mg/kg and more (P < 0.05). Respective thrombus weights in the control, 3, 10, and 30 mg/kg groups of YM150 were 4.8, 3.6, 2.4, and 2.0 mg. Aspirin alone inhibited thrombus formation, with significance at 100 mg/kg and more (P < 0.01). Respective thrombus weights in the control, 30, 100, and 300 mg/kg group of aspirin were 6.2, 4.2, 2.8, and 1.5 mg. Clopidogrel alone inhibited thrombus formation, with significance at 1 mg/kg and more (P < 0.01). Respective thrombus weights in the control, 0.3, 1, and 3 mg/kg group of clopidogrel were 4.8, 3.6, 2.9, and 1.3 mg. When administered concomitantly with 100 mg/kg of aspirin, YM150 (3, 10, 30 mg/kg) further inhibited thrombogenesis, with significance at 30 mg/kg of YM150 (P < 0.05) and thrombus weights of 2.4, 1.5, and 1.3 mg, respectively. When administered concomitantly with 1 mg/kg of clopidogrel, YM150 (3, 10, 30 mg/kg) further inhibited thrombogenesis, with significance at 30 mg/kg of YM150 (P < 0.05) and thrombus weights of 3.0, 2.0, and 1.5 mg, respectively. Collagen-induced platelet aggregation was reduced to 16.7% of the control level by 100 mg/kg of aspirin, and ADP-induced platelet aggregation was reduced to 74.4% of the control level by 1 mg/kg of clopidogrel. These effects were not changed in the presence of YM150. Prothrombin time and bleeding time were not prolonged by any of the agents alone, and further, these parameters were not affected by combined use of YM150 with either aspirin or clopidogrel. Conclusions: The thrombosis study suggests that both the platelet aggregation and coagulation cascade participate in thrombus formation in this model since both antiplatelet agents and the anticoagulant YM150 were effective. Thus, the thrombosis induced in this model can be considered similar to arterial thrombosis in humans where both platelets and fibrin are involved. Taken together, YM150 is a promising antithrombotic agent that augments the effects of antiplatelet agents against arterial thrombosis without increasing bleeding risk. Disclosures: Iwatsuki: Astellas Phama Inc.: Employment. Sakata:Astellas Phama Inc.: Employment. Moritani:Astellas Phama Inc.: Employment.

Стилі APA, Harvard, Vancouver, ISO та ін.

20

Lip, Gregory YH, and Eduard Shantsila. "Mechanisms of thrombogenesis in atrial fibrillation – Authors' reply." Lancet 373, no. 9668 (March 2009): 1006–7. http://dx.doi.org/10.1016/s0140-6736(09)60605-x.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

21

Gao, Shu-Ping, Xin-Tao Deng, Li-Jun Ge, Hong Luan, Jin-Guo Zheng, Chu Chen, Min-Hui Jiang, and Min Pan. "Is inflammation linked to thrombogenesis in atrial fibrillation?" International Journal of Cardiology 149, no. 2 (June 2011): 260–61. http://dx.doi.org/10.1016/j.ijcard.2011.02.046.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

22

Zhang, Ran, Hai-hong Ran, Yu-xiao Zhang, Cai-yi Lu, and Qiang Xu. "Impact of Rate and Rhythm on Atrial Thrombogenesis in Atrial Fibrillation." Journal of the American College of Cardiology 62, no. 2 (July 2013): 167. http://dx.doi.org/10.1016/j.jacc.2013.02.084.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

23

Watson, Timothy, Eduard Shantsila, and Gregory YH Lip. "Mechanisms of thrombogenesis in atrial fibrillation: Virchow's triad revisited." Lancet 373, no. 9658 (January 2009): 155–66. http://dx.doi.org/10.1016/s0140-6736(09)60040-4.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

24

Becker, Richard C. "Thrombogenesis in atrial fibrillation: contributing mechanisms and natural history." Journal of Thrombosis and Thrombolysis 26, no. 3 (October 19, 2008): 262–64. http://dx.doi.org/10.1007/s11239-008-0278-y.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

25

Becker, Richard C. "Thrombogenesis in atrial fibrillation contributing mechanisms and natural history." Journal of Thrombosis and Thrombolysis 27, no. 1 (January 2009): 119–21. http://dx.doi.org/10.1007/s11239-009-0307-5.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

26

Khan, Ahsan A., and Gregory Y. H. Lip. "The prothrombotic state in atrial fibrillation: pathophysiological and management implications." Cardiovascular Research 115, no. 1 (November 2, 2018): 31–45. http://dx.doi.org/10.1093/cvr/cvy272.

Повний текст джерела

Анотація:

AbstractAtrial fibrillation (AF) is the commonest sustained cardiac arrhythmia and is associated with significant morbidity and mortality. There is plenty of evidence available to support the presence of a prothrombotic or hypercoagulable state in AF, but the contributory factors are multifactorial and cannot simply be explained by blood stasis. Abnormal changes in atrial wall (anatomical and structural, as ‘vessel wall abnormalities’), the presence of spontaneous echo contrast to signify abnormal changes in flow and stasis (‘flow abnormalities’), and abnormal changes in coagulation, platelet, and other pathophysiologic pathways (‘abnormalities of blood constituents’) are well documented in AF. The presence of these components therefore fulfils Virchow’s triad for thrombogenesis. In this review, we present an overview of the established and professed pathophysiological mechanisms for thrombogenesis in AF and its management implications.

Стилі APA, Harvard, Vancouver, ISO та ін.

27

Kamath, S. "Platelet activation, haemorheology and thrombogenesis in acute atrial fibrillation: a comparison with permanent atrial fibrillation." Heart 89, no. 9 (September 1, 2003): 1093–95. http://dx.doi.org/10.1136/heart.89.9.1093.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

28

Lim, H., S. Willoughby, C. Gan, C. Schultz, D. Lau, D. Leong, M. Alasady, et al. "Left Atrial Thrombogenesis Due to Atrial Fibrillation: Is it Rate or Rhythm?" Heart, Lung and Circulation 19 (January 2010): S90. http://dx.doi.org/10.1016/j.hlc.2010.06.877.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

29

ROLDAN, V. "Interleukin-6, endothelial activation and thrombogenesis in chronic atrial fibrillation." European Heart Journal 24, no. 14 (July 2003): 1373–80. http://dx.doi.org/10.1016/s0195-668x(03)00239-2.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

30

Freestone, Bethan, Aun Yeong Chong, Hoong Sern Lim, Andrew Blann, and Gregory Y. H. Lip. "Angiogenic factors in atrial fibrillation: A possible role in thrombogenesis?" Annals of Medicine 37, no. 5 (January 2005): 365–72. http://dx.doi.org/10.1080/07853890510037392.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

31

Lip, G. Y. H., M. J. Metcalfe, A. Rumley, F. G. Dunn, and G. D. O. Lowe. "Cardioversion of Atrial Fibrillation Reduces Intravascular Fibrin Turnover and Thrombogenesis." Clinical Science 86, s30 (February 1, 1994): 34P. http://dx.doi.org/10.1042/cs086034p.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

32

Essa, Hani, Andrew M. Hill, and Gregory Y. H. Lip. "Atrial Fibrillation and Stroke." Cardiac Electrophysiology Clinics 13, no. 1 (March 2021): 243–55. http://dx.doi.org/10.1016/j.ccep.2020.11.003.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

33

Yamashita, Takeshi. "Stroke and atrial fibrillation." Nippon Ronen Igakkai Zasshi. Japanese Journal of Geriatrics 40, no. 4 (2003): 322–24. http://dx.doi.org/10.3143/geriatrics.40.322.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

34

Extramiana, Fabrice, and Pierre Maison-Blanche. "Stroke and Atrial Fibrillation." Stroke 46, no. 3 (March 2015): 605–7. http://dx.doi.org/10.1161/strokeaha.114.007809.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

35

Cheng, T. O. "Stroke and atrial fibrillation." Stroke 22, no. 8 (August 1991): 1086. http://dx.doi.org/10.1161/str.22.8.1086a.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

36

Nichols, E. H., and S. Messe. "Atrial Fibrillation and Stroke." MD Conference Express 14, no. 6 (June 1, 2014): 15–17. http://dx.doi.org/10.1177/155989771406010.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

37

Kaarisalo, Minna M., Pirjo Immonen-Räihä, Reijo J. Marttila, Veikko Salomaa, Esko Kaarsalo, Kalervo Salmi, Cinzia Sarti, Juhani Sivenius, Jorma Torppa, and Jaakko Tuomilehto. "Atrial Fibrillation and Stroke." Stroke 28, no. 2 (February 1997): 311–15. http://dx.doi.org/10.1161/01.str.28.2.311.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

38

Parnetti, L., and V. Gallai. "Atrial Fibrillation and Stroke." Cerebrovascular Diseases 10, no. 4 (2000): 40–41. http://dx.doi.org/10.1159/000047593.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

39

Giardina, MD, Elsa-Grace V. "Atrial Fibrillation and Stroke." American Journal of Cardiology 80, no. 4 (August 1997): 11D—18D. http://dx.doi.org/10.1016/s0002-9149(97)00580-8.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

40

Sherman, David G. "Atrial fibrillation and stroke." Journal of Stroke and Cerebrovascular Diseases 6, no. 4 (April 1997): 165–66. http://dx.doi.org/10.1016/s1052-3057(97)80002-x.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

41

Eisinger, A. J. "STROKE AND ATRIAL FIBRILLATION." Lancet 329, no. 8535 (March 1987): 743. http://dx.doi.org/10.1016/s0140-6736(87)90377-1.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

42

Anderson, David C., Richard L. Koller, Richard W. Asinger, Scott R. Bundlie, and Lesly A. Pearce. "ATRIAL FIBRILLATION AND STROKE." Neurologist 4, no. 5 (September 1998): 235–58. http://dx.doi.org/10.1097/00127893-199809000-00001.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

43

Healey, Jeff S., Guy Amit, and Thalia S. Field. "Atrial fibrillation and stroke." Current Opinion in Neurology 33, no. 1 (February 2020): 17–23. http://dx.doi.org/10.1097/wco.0000000000000780.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

44

Mulpuru, Siva K., Alejandro A. Rabinstein, and Samuel J. Asirvatham. "Atrial Fibrillation and Stroke." Cardiac Electrophysiology Clinics 6, no. 1 (March 2014): 31–41. http://dx.doi.org/10.1016/j.ccep.2013.11.001.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

45

DeSimone, Christopher V., Malini Madhavan, Elisa Ebrille, Alejandro A. Rabinstein, Paul A. Friedman, and Samuel J. Asirvatham. "Atrial Fibrillation and Stroke." Cardiac Electrophysiology Clinics 6, no. 1 (March 2014): 87–94. http://dx.doi.org/10.1016/j.ccep.2013.11.003.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

46

Asirvatham, Samuel J., Ranjan K. Thakur, and Andrea Natale. "Stroke in Atrial Fibrillation." Cardiac Electrophysiology Clinics 6, no. 1 (March 2014): xiii—xiv. http://dx.doi.org/10.1016/j.ccep.2013.12.001.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

47

Brainin, Michael. "Atrial fibrillation and stroke." World Stroke Academy 1, no. 5 (September 2013): 25. http://dx.doi.org/10.1002/wsa2.20016.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

48

Hart, Robert G., and Jonathan L. Halperin. "Atrial Fibrillation and Stroke." Stroke 32, no. 3 (March 2001): 803–8. http://dx.doi.org/10.1161/01.str.32.3.803.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

49

Proietti, Marco, and Gregory Y. H. Lip. "Atrial Fibrillation and Stroke." Cardiology Clinics 34, no. 2 (May 2016): 317–28. http://dx.doi.org/10.1016/j.ccl.2015.12.006.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

50

Albers, Gregory W. "Atrial Fibrillation and Stroke." Archives of Internal Medicine 154, no. 13 (July 11, 1994): 1443. http://dx.doi.org/10.1001/archinte.1994.00420130030006.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Ми пропонуємо знижки на всі преміум-плани для авторів, чиї праці увійшли до тематичних добірок літератури. Зв'яжіться з нами, щоб отримати унікальний промокод!